Mutations in glucose transporter 9 gene SLC2A9 cause renal hypouricemia.

Renal hypouricemia is an inherited disorder characterized by impaired renal urate (uric acid) reabsorption and subsequent low serum urate levels, with severe complications such as exercise-induced acute renal failure and nephrolithiasis. We previously identified SLC22A12, also known as URAT1, as a causative gene of renal hypouricemia. However, hypouricemic patients without URAT1 mutations, as well as genome-wide association studies between urate and SLC2A9 (also called GLUT9), imply that GLUT9 could be another causative gene of renal hypouricemia. With a large human database, we identified two loss-of-function heterozygous mutations in GLUT9, which occur in the highly conserved "sugar transport proteins signatures 1/2." Both mutations result in loss of positive charges, one of which is reported to be an important membrane topology determinant. The oocyte expression study revealed that both GLUT9 isoforms showed high urate transport activities, whereas the mutated GLUT9 isoforms markedly reduced them. Our findings, together with previous reports on GLUT9 localization, suggest that these GLUT9 mutations cause renal hypouricemia by their decreased urate reabsorption on both sides of the renal proximal tubules. These findings also enable us to propose a physiological model of the renal urate reabsorption in which GLUT9 regulates serum urate levels in humans and can be a promising therapeutic target for gout and related cardiovascular diseases.

Mobile and accurate detection system for infection by the 2009 pandemic influenza A (H1N1) virus with a pocket-warmer reverse-transcriptase loop-mediated isothermal amplification.

The 2009 pandemic H1N1 influenza A virus spread quickly worldwide in 2009. Since most of the fatal cases were reported in developing countries, rapid and accurate diagnosis methods that are usable in poorly equipped laboratories are necessary. In this study, a mobile detection system for the 2009 H1N1 influenza A virus was developed using a reverse-transcriptase loop-mediated isothermal amplification (RT-LAMP) kit with a disposable pocket-warmer as a heating device (designated as pwRT-LAMP). The pwRT-LAMP can detect as few as 100 copies of the virus--which is nearly as sensitive as real-time reverse-transcription polymerase chain reaction (RT-PCR)--and does not cross-react with RNA of seasonal influenza viruses. To evaluate the usefulness of the pwRT-LAMP system, nasal swab samples were collected from 56 patients with flu-like symptoms and were tested. Real-time RT-PCR confirmed that the 2009 H1N1 influenza A virus was present in 27 of the 56 samples. Of these 27 positive samples, QuickVue Influenza A+B immunochromatography detected the virus in only 11 samples (11/27; 40.7%), whereas the pwRT-LAMP system detected the virus in 26 of the 56 samples (26/27 of the positive samples; 96.3%). These findings indicate that the mobile pwRT-LAMP system is an accurate diagnostic system for the 2009 H1N1 influenza A virus, and has great potential utility in diagnosing future influenza pandemics.

Voltage-gated potassium channel Kv1.3 blocker as a potential treatment for rat anti-glomerular basement membrane glomerulonephritis.

The voltage-gated potassium channel Kv1.3 has been recently identified as a molecular target that allows the selective pharmacological suppression of effector memory T cells (T(EM)) without affecting the function of naïve T cells (T(N)) and central memory T cells (T(CM)). We found that Kv1.3 was expressed on glomeruli and some tubules in rats with anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). A flow cytometry analysis using kidney cells revealed that most of the CD4(+) T cells and some of the CD8(+) T cells had the T(EM) phenotype (CD45RC(-)CD62L(-)). Double immunofluorescence staining using mononuclear cell suspensions isolated from anti-GBM GN kidney showed that Kv1.3 was expressed on T cells and some macrophages. We therefore investigated whether the Kv1.3 blocker Psora-4 can be used to treat anti-GBM GN. Rats that had been given an injection of rabbit anti-rat GBM antibody were also injected with Psora-4 or the vehicle intraperitoneally. Rats given Psora-4 showed less proteinuria and fewer crescentic glomeruli than rats given the vehicle. These results suggest that T(EM) and some macrophages expressing Kv1.3 channels play a critical role in the pathogenesis of crescentic GN and that Psora-4 will be useful for the treatment of rapidly progressive glomerulonephritis.

Doppler phase-shifting digital holography and its application to surface shape measurement.

Digital holography utilizing the optical Doppler effect is proposed in which the time variation of interference fringes is recorded using a high-speed CMOS camera. The complex amplitude diffracted from the object wave is extracted by time-domain Fourier transforming the recorded interference fringes. The method was used to measure the surface shape of a concave mirror under a disturbed environment.

Elevated urinary plasmin activity resistant to alpha2-antiplasmin in acute poststreptococcal glomerulonephritis.

BACKGROUND: A pathogenic role of intraglomerular plasmin bound to nephritogenic antigen (nephritis-associated plasmin receptor, NAPlr) and resistant to physiologic inhibitors such as alpha(2)-antiplasmin (alpha(2)-AP) has recently been proposed in acute poststreptococcal glomerulonephritis (APSGN). To confirm this concept, we analysed the urinary profile of plasmin cascade in APSGN patients. METHODS: Urine samples from 10 patients with APSGN, 12 patients with IgA nephropathy (IgAN), 10 patients with streptococcal infection without nephritis (SI) and 10 healthy control subjects were analysed. The alpha(2)-AP-resistant plasmin activity was assessed by a chromogenic assay after alpha(2)-AP was added to each urine sample. Urinary plasminogen activator (PA) and plasmin were further analysed by polyacrylamide gel zymography. Urinary NAPlr was assessed by western blot analysis in selected samples. RESULTS: Urinary alpha(2)-AP-resistant plasmin activity corrected for creatinine concentration (units/g x creatinine) was significantly higher in patients with APSGN (2.99 +/- 0.63) than in patients with IgAN (1.02 +/- 0.20, P < 0.01), SI (0.79 +/- 0.17, P < 0.01), or in healthy control subjects (0.73 +/- 0.18, P < 0.01). This tendency was confirmed by casein gel zymography. However urinary PA activity assessed by plasminogen-casein gel zymography did not differ between groups. NAPlr was detected in the urine of APSGN patients. CONCLUSIONS: We found elevated urinary plasmin activity resistant to alpha(2)-AP, which may be due to urinary excretion of NAPlr in patients with APSGN. This result supports the pathogenic role of the NAPlr-plasmin complex in the development of APSGN. Furthermore, alpha(2)-AP-resistant urinary plasmin activity may be useful as a diagnostic marker for APSGN.

A Rho-kinase inhibitor, fasudil, prevents development of diabetes and nephropathy in insulin-resistant diabetic rats.

Fasudil, a Rho-kinase inhibitor, may improve insulin signaling. However, its long-term effect on metabolic abnormalities and its preventive effect on diabetic nephropathy are still unknown. We assessed these effects of fasudil in insulin-resistant diabetic rats, comparing them with those of an angiotensin II receptor blocker, olmesartan. Male Otsuka Long-Evans Tokushima fatty (OLETF) and Long-Evans Tokushima Otsuka, non-diabetic control, rats at 15 weeks of age were used. OLETF rats were randomized to receive a low or a high dose of fasudil or olmesartan for 25 weeks. To examine the therapeutic effects after the development of diabetes, OLETF rats at 30 weeks of age were given fasudil for 10 weeks. Administration of high-dose fasudil completely suppressed the development of diabetes, obesity, and dyslipidemia and increased serum adiponectin levels in OLETF rats. High-dose olmesartan also decreased hemoglobin A1c and increased serum adiponectin. There was a significant correlation between hemoglobin A1c and serum adiponectin or free fatty acid levels. The treatment with high-dose fasudil ameliorated proteinuria, glomerulosclerosis, renal interstitial fibrosis, and macrophage infiltration in OLETF rats. Olmesartan, even at the low dose, suppressed renal complications. The treatment with fasudil after the development of diabetes improved the metabolic abnormalities in OLETF rats, but could not suppress the progression of nephropathy. We conclude that the long-term treatment with fasudil prevents the development of diabetes, at least in part, by improving adipocyte differentiation in insulin-resistant diabetic rats. Early use of fasudil may prevent diabetic nephropathy.

Effects of renin-angiotensin system blockade on macrophage infiltration in patients with hypertensive nephrosclerosis.

The mechanisms of hypertensive nephrosclerosis are not fully understood. In experimental models of the disease, inflammatory reactions such as macrophage infiltration play an important role. In human hypertensive nephrosclerosis, however, there have been few studies examining the role of inflammation histologically. We investigated whether the number of infiltrating macrophages was increased in human hypertensive nephrosclerosis, and evaluated the effects of a blockade of the renin-angiotensin system on clinical and histological findings. We examined macrophage infiltration using immunohistochemistry in renal biopsy specimens obtained from 16 patients with hypertensive nephrosclerosis, 5 patients with IgA nephropathy, 5 patients with membranous nephropathy, and 5 patients with minimal change nephrotic syndrome. The number of infiltrating macrophages in glomeruli was significantly larger in the patients with hypertensive nephrosclerosis than in those with minimal change nephrotic syndrome. The patients with hypertensive nephrosclerosis were divided into groups based on their use of antihypertensive agents at the time of renal biopsy. We investigated the effects of antihypertensive agents on clinical findings, macrophage infiltration, and monocyte chemoattractant protein-1 expression. There was no difference in clinical findings between the hypertensive groups. The numbers of infiltrating macrophages and monocyte chemoattractant protein-1-positive cells in glomeruli were significantly smaller in patients treated with an angiotensin-converting enzyme inhibitor or angiotensin II type 1 receptor blocker, whereas calcium channel blockers had no influence on histological findings. In conclusion, inflammation is involved in the progression of human hypertensive nephrosclerosis and the inflammatory process is inhibited by blocking the renin-angiotensin system.

Involvement of transglutaminase-2 in pathological changes in renal disease.

BACKGROUND: Transglutaminase (Tg)-2 is shown to be related to renal fibrosis. However, its roles in human kidney disease have not been fully studied. METHODS: Using immunohistochemistry, we examined Tg-2 expression in renal biopsy specimens from 22 patients with IgA nephropathy (IgAN) and correlated the intensity of Tg-2 staining with clinical and histopathological parameters. We compared the distribution and intensity of Tg-2 staining with those of transforming growth factor (TGF)-beta staining. RESULTS: In normal human kidneys, Tg-2 staining was not significant. In IgAN kidneys, glomerular Tg-2 staining correlated with serum creatinine (S-Cr), creatinine clearance (Ccr), urinary protein excretion, glomerular sclerosis, and mesangial cell proliferation. Tubulointerstitial Tg-2 correlated with S-Cr, Ccr, N-acetyl-beta-glucosaminidase, urinary beta(2)-microglobulin, and tubulointerstitial injuries. Tg-2 staining in the vicinity of vascular poles of glomeruli preceded the development of mesangial lesions, and was more remarkable in cases with renal impairment. The distribution and intensity of Tg-2 staining were not consistent with those of TGF-beta staining. In glomerular crescents, Tg-2 staining was remarkable. CONCLUSION: The present study showed a correlation between Tg-2 expression and renal function and pathological changes. Tg-2 expression in the vicinity of vascular poles was notable because that may be an initial marker of glomerular injury.

Maintaining of the Green Fluorescence Emission of 9-Aminoanthracene for Bioimaging Applications.

The green fluorescence emission of 9-aminoanthracence (9AA) was maintained by controlling the oxidation of 9AA with oxygen in the solid state and in solution. The solid-state fluorescence of 9AA was maintained for a longer time when lauric acid was used because the equilibrium between 9AA and 9-anthrylammonium salt (9AAH + ) inclines toward the right-hand side in the presence of an acid. A solution of 9AA in CDCl3, to which nitrogen had been bubbled through for 5 min, continued to emit green fluorescence for more than 3 days, whereas the fluorescence emission disappeared within 3 days for the solution that had been bubbled with oxygen for 5 min. 9AA is oxidized by oxygen in MeOH under dark conditions to give almost nongreen fluorescent anthraquinone monoimine (AQNH), whereas dimerization of 9AA occurs under UV irradiation at 365 nm, much faster than the generation of AQNH. These results suggest that 9AA is oxidized by the triplet rather than the singlet oxygen in MeOH. Some of the organic molecules, proteins, and biological tissues were successfully stained with 9AA on microscope slides within 10 min because the green fluorescence emission of 9AA was successfully maintained in the presence of an acid and under hypoxic conditions of the used materials.

Impact of hypertension and hypertension-related vascular lesions in IgA nephropathy.

It remains poorly understood whether vascular pathology plays an important role in the progression of renal parenchymal disease in humans. Moreover, in the case of hypertensive patients with mild proteinuria, nephrologists tend to make a diagnosis of benign nephrosclerosis without renal biopsy. Among 172 patients who were treated at our hospital for biopsy-proven IgA nephropathy, we performed quantitative histopathological analysis in 38 patients with mild proteinuria of less than 0.5 g/day. We related these histopathological parameters with clinical data at biopsy and also with follow-up data. The percentage of glomeruli showing global sclerosis exceeded 10% of total glomeruli in 15 of the patients (39.5%) and exceeded 20% in 9 (23.7%). Arteriosclerosis and tubulointerstitial changes significantly correlated with glomerular sclerosis, but mesangial cell proliferation did not. Among the 38 patients, the 12 with hypertension showed more severe glomerular sclerosis, tubulointerstitial changes and arteriosclerosis compared with the 26 without hypertension, but the mesangial cell proliferation was identical between the two groups. Stepwise multiple regression analysis revealed that hypertension and urinary protein excretion (UPE) were independent risk factors for arteriosclerosis. The follow-up data of a mean period of 27.6 months showed that 9 of the 38 patients (23.7%) had an increase in UPE. Hypertension, arteriosclerosis, age, and UPE at biopsy were selected as the important risk factors for an increase in UPE in the follow-up. Our results provide not only clinical but histopathological evidence that hypertension affects the prognosis of mild proteinuric nephropathy through vascular lesions.

A case of essential thrombocytosis developing nephrotic syndrome and severe endothelial damage.

We present a 75-year-old Japanese man with essential thrombocytosis presenting nephrotic syndrome. Proteinuria developed soon after the patient was given a diagnosis of essential thrombocytosis and, 4 years later, it increased to a nephrotic range. Renal biopsy revealed one third of the obtained glomeruli totally sclerotic and the other glomeruli showed a marked thickening of the glomerular basement membrane and mild mesangial proliferation. Remarkable widening of the subendothelial space was evident on electron microscopy. Increased expression of platelet derived growth factor receptor beta was detected in the mesangium and interstitium by immunohistochemistry. Abnormal platelet activation in myeloproliferative disease has been shown to contribute in glomerulosclerosis by releasing various growth factors and cytokines including PDGF. Considering his clinical course and the pathological findings, the probable risk factor for developing severe endothelial damage and glomerulosclerosis is due to the persistence of high platelet count and platelet abnormality.

Mutations in human urate transporter 1 gene in presecretory reabsorption defect type of familial renal hypouricemia.

To date, 11 loss of function mutations in the human urate transporter 1 (hURAT1) gene have been identified in subjects with idiopathic renal hypouricemia. In the present studies we investigated the clinical features and the mutations in the hURAT1 gene in seven families with presecretory reabsorption defect-type renal hypouricemia and in one family with the postsecretory reabsorption defect type. Twelve affected subjects and 26 family members were investigated. Mutations were analyzed by PCR and the direct sequencing method. Urate-transporting activities of wild-type and mutant hURAT1 were determined by [14C]urate uptake in Xenopus oocytes. Mutational analysis revealed three previously reported mutations (G774A, A1145T, and 1639-1643 del-GTCCT) and a novel mutation (T1253G) in families with the presecretory reabsorption defect type. Neither mutations in the coding region of hURAT1 gene nor significant segregation patterns of the hURAT1 locus were detected in the postsecretory reabsorption defect type. All hURAT1 mutants had significantly reduced urate-transporting activities compared with wild type (P < 0.05; n = 12), suggesting that T1253G is a loss of function mutation, and hURAT1 is responsible for the presecretory reabsorption defect-type familial renal hypouricemia. Future studies are needed to identify a responsible gene for the postsecretory reabsorption defect-type familial renal hypouricemia.

An adult with acute poststreptococcal glomerulonephritis complicated by hemolytic uremic syndrome and nephrotic syndrome.

We report the case of a 47-year-old man with the simultaneous occurrence of clinical and laboratory features consistent with acute poststreptococcal glomerulonephritis (APSGN), hemolytic uremic syndrome (HUS), and nephrotic syndrome. Acute nephritic syndrome occurred 3 weeks after having pharyngeal pain and diarrhea. He presented with edema and hypertension on admission. Laboratory evaluation showed hemolytic anemia with fragmentation, thrombocytopenia, elevated lactic dehydrogenase level, low haptoglobin level, low complement C3 level, and elevated antistreptolysin-O titer. Serum creatinine level was 1.22 mg/dL (108 micromol/L), and urinalysis showed marked proteinuria, with protein of 8.7 g/d, and hematuria. The renal biopsy specimen was characteristic of APSGN, but not HUS. Moderate expansion of the mesangial matrix, moderate proliferation of epithelial and endothelial cells, and marked infiltration of neutrophils was seen by means of light microscopy, and many subepithelial humps were seen by means of electron microscopy. Neither fibrin deposition nor evidence of thrombotic microangiopathy was found. Complement C3 deposition along the capillary wall and tubules was seen in an immunofluorescence study. The patient was administered plasma infusion at 320 mL/d and antihypertensive drugs. Serum complement C3 and haptoglobin levels returned to normal within 3 weeks. This is a rare case of the simultaneous occurrence of APSGN, HUS, and nephrotic syndrome.

Correlation between the resistive index by Doppler ultrasound and kidney function and histology.

BACKGROUND: Although duplex Doppler ultrasonography has been used widely, it still is unknown whether resistive index could be related directly to vascular or tubulointerstitial changes in the kidney. METHODS: Thirty-three patients who underwent renal biopsy were included in the present study. Clinical data, including sex; age; time from abnormal urinalysis result to biopsy; serum creatinine level; creatinine clearance; urinary excretion of protein, N-acetyl-beta-glucosaminidase, and urinary beta2-microglobulin; and presence of hypertension, were recorded at biopsy. Histopathologic data, including glomerular sclerosis, interstitial fibrosis/tubular atrophy, interstitial infiltration, and arteriolosclerosis, were evaluated separately by means of a quantitative or semiquantitative method. We examined whether resistive index at biopsy was related to these clinical and histopathologic parameters and, moreover, to renal outcome in patients followed up for more than 2 years. RESULTS: Age, creatinine clearance, urinary beta2-microglobulin excretion, and all histopathologic parameters showed statistically significant correlations with resistive index. However, stepwise multiple regression analysis showed that only arteriolosclerosis was chosen as an independent risk factor for increased resistive index. During the follow-up period of 57.5 +/- 15.6 months in 29 patients, 8 patients (27.6%) had progression of renal impairment, defined as an increase in serum creatinine level greater than 50%. They had a significantly increased resistive index at biopsy compared with patients without progression. CONCLUSION: We show a direct relationship between resistive index and arteriolosclerosis in damaged kidneys. Resistive index at renal biopsy may be useful as one of the prognostic markers for renal outcome.

Role of Coronary Calcium Scoring in the Assessment of Physiological Ischemia in Patients with Intermediate Stenosis.

Although coronary artery calcium (CAC) is an established marker of coronary atherosclerosis, whether it also reflects the physiological significance is unknown. This study aims to evaluate if CAC could indicate physiological ischemia in intermediate stenosis defined by an invasive fractional flow reserve (FFR). CAC score (CACS) derived from either whole coronary arteries or individual arteries was measured by computed tomography among patients with intermediate de novo lesions (percent diameter stenosis from 30% to less than 70%). All stenoses were evaluated by invasive FFR; lesions with an FFR ≤ 0.80 were considered significant. We enrolled 119 patients with 143 lesions. Of these, 42 lesions (29.4%) demonstrated significant ischemia by FFR measurement. FFR values had modest but significant correlations with CACS in individual arteries with intermediate stenosis (r = - 0.290; p < 0.001). A receiver operating characteristic curve analysis showed that CACS of individual arteries with intermediate stenosis had 71.4% sensitivity and 67.3% specificity as a predictor of significant ischemia at a cut off value of 145.9. Multivariable analysis showed that percent diameter stenosis and CACS in individual arteries with intermediate stenosis were independent predictors for significant ischemia. By net reclassification improvement analysis, CACS in individual arteries with intermediate stenosis provided incremental prediction for significant ischemia over minimum lumen diameter, percent diameter stenosis, and lesion length. CACS measured in each artery, but not the total CACS, provides additional information as to whether an angiographically intermediate stenosis within the artery is significant enough to cause myocardial ischemia.

Uncommon presentation of drug-refractory pacemaker-mediated common atrioventricular nodal reentrant tachycardia and a simple solution by reprogramming.

An 81-year-old woman who had undergone dual chamber pacemaker implantation for sick sinus syndrome was referred to our hospital with drug-refractory common atrioventricular (AV) nodal reentrant tachycardia. Ventricular pacing (Vp) following premature atrial contraction (PAC) with a long AV interval induced ventriculoatrial (VA) conduction, which allowed the tachycardia to be initiated. The sensed AV interval was shortened to 80 ms, allowing Vp during the refractory period of VA conduction. Postventricular atrial refractory period was shortened to 180 ms to sense PACs with short coupling interval. After reprogramming, the suppression of the tachycardia by blocking VA conduction following Vp was confirmed.

Fractalkine and its receptor, CX3CR1, upregulation in streptozotocin-induced diabetic kidneys.

BACKGROUND: Fractalkine is induced on activated endothelial cells and promotes strong adhesion of T cells and monocytes via its receptor CX3CR1. In kidney, fractalkine expression might be induced by high shear stress and play an important role in prolonged glomerular diseases. We examined whether fractalkine and CX3CR1 upregulation are found in streptozotocin-induced diabetic kidneys. METHODS: Diabetic rats were randomized to receive an angiotensin-converting enzyme inhibitor (temocapril), aminoguanidine or no treatment. Reverse transcription-competitive polymerase chain reaction, Western blot analysis and immunohistochemistry were used. RESULTS: At 4 weeks, fractalkine and CX3CR1 mRNA expression in diabetic kidneys increased compared with that in controls. Fractalkine staining in diabetic kidneys was clearly detected, along with glomerular capillary lumen and peritubular capillaries. A few CX3CR1 positive cell infiltration in diabetic glomeruli were found. Treatment with temocapril or aminoguanidine did not affect these changes. At 8 weeks, fractalkine and CX3CR1 mRNA expression in untreated diabetic kidneys markedly increased compared with that in controls. Membrane-anchored fractalkine protein expression in untreated diabetic rats also increased. The increased expression was suppressed by the treatment with temocapril and aminoguanidine. Increased CX3CR1-positive cell infiltration in diabetic glomeruli was also inhibited by both treatments. Some CX3CR1-positive cells were ED3 positive. CONCLUSIONS: Fractalkine and CX3CR1 upregulation were demonstrated in an early stage of diabetic kidney. These upregulation, as well as urinary albumin excretion, were suppressed by treatments with temocapril and aminoguanidine for 8 weeks. These findings suggest that fractalkine expression and CX3CR1-positive cell infiltration in diabetic kidneys might play an important role for progression of diabetic nephropathy.

[Pathological analysis of renal diseases with mild proteinuria].

Proteinuria is an important predictor of renal outcome in a variety of renal diseases. Proteinuria exceeding 0.5 g/day is often considered to be a major indication of renal biopsy. In this study, we analyzed the clinical and histopathological data of 58 patients with mild proteinuria of less than or equal to 0.5 g/day. The histopathological diagnosis included 45 cases(77.6%) of mesangial proliferative glomerulonephritis, 4 cases(6.9%) of lupus nephritis, one case of membranoproliferative glomerulonephritis and only 6 cases(10.3%) of minor glomerular abnormality. The percent sclerotic glomeruli exceeded 10% in 17 cases(29.3%) and reached 71.4% in 2 cases. There were no significant differences in histopathological parameters(percent sclerotic glomeruli, tubulointerstitial change, arterio-arterio sclerotic change) between the groups with or without microhematuria. There was a positive correlation between age and percent sclerotic glomeruli. Percent sclerotic glomeruli in our cases were higher than in the healthy population reported by Kaplan et al. and the influence of glomerulonephropathy was obvious. During the follow-up period(mean 19.7 months), one patient progressed to chronic renal failure and 2 patients had increased urinary protein excretion, but the others did not. These results suggest the importance of clarifying the prognosis by renal biopsy even in cases with mild proteinuria.

Tuberculous cellulitis in a patient with chronic kidney disease and polymyalgia rheumatica.

An 89-year-old man with advanced renal failure, polymyalgia rheumatica and a past history of tuberculosis was admitted with a high fever. Erythema and swelling appeared in the femoral region. Since the cellulitis failed to respond to antibiotic therapy, a skin biopsy was performed. The specimen showed the presence of epithelioid cell granuloma and panniculitis. Acid-fast organisms were found on Ziehl-Neelsen staining. A polymerase chain reaction test of tuberculosis was positive. Although a diagnosis of miliary tuberculosis was suggested, examinations of a bone marrow biopsy and fundoscopy revealed normal results. The patient's symptoms improved following treatment with isoniazid, rifampicin and ethambutol. This case represents an unusual presentation of tuberculous cellulitis in an immunocompromised patient.